Monoamine oxidases (MAO) in the pathogenesis of heart failure and ischemia/reperfusion injury

Nina Kaludercic, Andrea Carpi, Roberta Menabò, Fabio Di Lisa, Nazareno Paolocci

Research output: Contribution to journalReview articlepeer-review

107 Scopus citations


Recent evidence highlights monoamine oxidases (MAO) as another prominent source of oxidative stress. MAO are a class of enzymes located in the outer mitochondrial membrane, deputed to the oxidative breakdown of key neurotransmitters such as norepinephrine, epinephrine and dopamine, and in the process generate H2O2. All these monoamines are endowed with potent modulatory effects on myocardial function. Thus, when the heart is subjected to chronic neuro-hormonal and/or peripheral hemodynamic stress, the abundance of circulating/tissue monoamines can make MAO-derived H2O2 production particularly prominent. This is the case of acute cardiac damage due to ischemia/reperfusion injury or, on a more chronic stand, of the transition from compensated hypertrophy to overt ventricular dilation/pump failure. Here, we will first briefly discuss mitochondrial status and contribution to acute and chronic cardiac disorders. We will illustrate possible mechanisms by which MAO activity affects cardiac biology and function, along with a discussion as to their role as a prominent source of reactive oxygen species. Finally, we will speculate on why MAO inhibition might have a therapeutic value for treating cardiac affections of ischemic and non-ischemic origin. This article is part of a Special Issue entitled: Mitochondria and Cardioprotection.

Original languageEnglish (US)
Pages (from-to)1323-1332
Number of pages10
JournalBiochimica et Biophysica Acta - Molecular Cell Research
Issue number7
StatePublished - Jul 2011


  • Heart failure
  • Mitochondria
  • Monoamine oxidase
  • Myocardial injury
  • Reactive oxygen species

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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